Influenza A viruses are the causative agents of severe respiratory diseases resulting in significant morbidity and mortality. Most of the fatal cases in the course of an influenza virus (IV) infection are actually a result of secondary pneumonia caused by different bacteria, such as Staphylococcus aureus (S. aureus), Streptococcus pneumoniae and Haemophilus influenzae (Morens et al., 2008, Chertow et al., 2013). The most striking problems of bacterial co-infection are the suddenly increased pathogenicity (lwao et al., 2012, Paddock et al., 2012, Parker et al., 2012) and a limited arsenal of potent anti-infectives against the different pathogens. The high variability of influenza viruses and the continous emergence of new strains (Neumann et al., 2009,Taubenberger et al., 2010, Parry, 2013), specific characteristics of the bacterial strains (Grundmann et al., 2006, Moran et al., 2006, Gillet et al., 2007, Shilo et al., 2011), as well as the rapid resistance development of both, influenza viruses (Hayden et al., 1992, Bright et al., 2006, Pinto et al., 2006, De Clercq et al., 2007, Pinto et al, 2007) and bacteria (Grundmann et al., 2006, Moran et al., 2006, Shilo et al., 2011) against the available drugs/antibiotics are the major reasons for the poor treatment options. Moreover, it is incidental that treatment of coinfections with influenza viruses and bacteria is not possible with a single compound, so far. The current invention solves this problem in that it proposes a novel anti-infective strategy against IV and S. aureus co-infections by using single drugs. Furthermore, the present invention solves the problem of rapid resistence development of bacteria by providing drug that targets cellular factors rather than the bacterium itself.